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Inhibition of IL-17 Alleviates Blood-Brain Barrier Disruption Following Diffuse Axonal Injury Accompanied by
Zhiguo Xing1,2, Xing Wei3, Ming Zhang4
1Department of Neurosurgery, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, 710061, China, xjtu.edu.cn.
Mediators of Inflammation
|May 28, 2026
Summary
Interleukin-17A (IL-17) exacerbates blood-brain barrier (BBB) breakdown and axonal injury in hyperglycemia after diffuse axonal injury (DAI). Inhibiting IL-17 protects the BBB and reduces neuroinflammation and oxidative stress.
Area of Science:
- Neuroscience
- Immunology
- Cell Biology
Background:
- Hyperglycemia (HG) complicates outcomes following diffuse axonal injury (DAI).
- The role of interleukin-17A (IL-17) in hyperglycemia-induced blood-brain barrier (BBB) breakdown post-DAI remains unclear.
Purpose of the Study:
- To elucidate the effects and mechanism of IL-17 in hyperglycemia-induced BBB breakdown following DAI.
- To investigate IL-17 as a potential therapeutic target for neurovascular damage in hyperglycemic DAI.
Main Methods:
- Proteomic analysis (4D-SmartDIA) identified differentially expressed proteins in high-glucose stimulated cells.
- Established rat models of DAI and hyperglycemia, assessing IL-17/IL-17R expression, BBB permeability, axonal injury, glial response, apoptosis, inflammation, and oxidative stress.
- Inhibited the IL-17 pathway using suberoylanilide hydroxamic acid (SAHA) to evaluate its protective effects and impact on the NF-κB pathway.
Main Results:
- Proteomics revealed IL-17 signaling as a significantly enriched pathway in high-glucose conditions.
- Elevated IL-17 and IL-17R expression (localized to vascular endothelial cells) was observed post-DAI, further enhanced by hyperglycemia.
- Hyperglycemia aggravated axonal injury, BBB disruption, inflammation, and oxidative stress; IL-17 inhibition reversed these effects and protected BBB integrity via NF-κB pathway modulation.
Conclusions:
- IL-17 mediates hyperglycemia-induced axonal injury following DAI by compromising BBB integrity through NF-κB-dependent inflammation and oxidative stress.
- IL-17 inhibition offers a promising therapeutic strategy for mitigating neurovascular damage in hyperglycemic DAI patients.
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